Sleep apnea, a prevalent sleep disorder, manifests many undesirable symptoms that range from snoring, cessation of breathing, and headaches to depression, memory loss, and exacerbation of heart disease. “Hypopnea,” a related malady that begets some of the same symptoms as apnea, refers to a breathing rate or tidal volume that is less than fifty percent of a patient's normal baseline breathing pattern.
Blood chemistry changes occur when apnea and hypopnea modify normal breathing during sleep. Breathing difficulty can cause blood oxygenation to fall to low levels and carbon dioxide and its derivatives to build up in the blood. When the control centers in the brain sense these chemical changes they often cause an arousal of the apneic patient. Thereafter, regular breathing and normal exchange of oxygen and accumulated carbon dioxide may resume—for a time, until the next episode.
Severe apnea and hypopnea result in hundreds of episodes of low oxygen levels per night. The typical apnea patient may have little awareness of the nightly struggle to breathe until its effects are felt the next day.
Sleep apnea can be classified as “obstructive” if caused by mechanical blockage of airflow, “central” if caused by central nervous system disorder, or “mixed” if a combination of obstructive and central.
Sleep apnea can be life-threatening if it occurs with coronary artery disease (CAD) or congestive heart failure (CHF—sometimes referred to as just “heart failure”). Not only does apnea directly place a load on the heart and cardiopulmonary system, but indirectly affects these organs by circumventing restful sleep. Alteration of sleep cycle phases causes sleep to be partly ineffective. A cycle of sleep debt and daytime weariness worsens CAD, CHF, and also hypertension. Consequently, sleep apneics who have a blood oxygen level lowered by sleep-disordered breathing are at increased risk for hypertension, arrhythmias, heart attack, stroke, and nocturnal sudden death.
Sleep apnea burden (“apnea burden”) is a metric that may be defined in several ways. For example, the apnea burden may be proportional to the number of apneic and hypopneic episodes that occur per hour, sometimes called the Apnea Hypopneic Index (AHI). Other metrics of apnea burden are possible—for example, the total time spent in apnea and hypopnea per hour, the total time spent in apnea and hypopnea per night, or the frequency of arousal due to apnea and hypopnea per hour. In general, as used herein, “apnea burden” means the extent, severity, and/or gravity of the sleep apnea/hypopnea that a patient experiences, and is described in U.S. Pat. No. 6,741,885 to Park et al., entitled, “Implantable Cardiac Device for Managing the Progression of Heart Disease and Method,” which is incorporated by reference herein.
Approximately fifty percent of patients with heart failure suffer concurrent sleep apnea. About ten percent of these heart failure patients suffer from obstructive sleep apnea, while about forty percent suffer from central sleep apnea. A high comorbidity exists between sleep apnea and CHF, which results from a negative synergy between problematic gas exchange during apnea and problematic oxygen distribution caused by weak cardiac pumping and fluid buildup characteristic of CHF.
CHF is a condition in which a weakened heart cannot provide enough pressure to prevent buildup of fluid in bodily tissues. CHF may affect either the right side, left side, or both sides of the heart. The weak pumping action causes fluid to back up into other areas of the body including the liver, gastrointestinal tract, and extremities (right-sided heart failure), or the lungs (left-sided heart failure). Heart failure patients have characteristic pulmonary edema or pitting edema of the lower legs.
Structural and functional causes of heart failure include high blood pressure (hypertension), valvular heart disease, congenital heart disease, cardiomyopathy, heart tumor, and other heart diseases. Precipitating and exacerbating factors include infections with high fever, anemia, irregular heartbeats (arrhythmias), hyperthyroidism, and kidney disease, and of course, sleep apnea. CHF and sleep apnea often occur together in a patient, as mentioned above, and exacerbate each other. Conversely, treating one usually improves the other.
Separately or in addition to the exemplary methods described herein, sleep apnea may be treated by administering continuous positive airway pressure (CPAP) or by various other treatments, such as surgery and medications. The type of treatment depends in part on the type of sleep apnea and personal preferences. It is generally believed that reducing heart failure symptoms reduces the apnea burden, which in turn further reduces the heart failure symptoms. Cardiac pacing therapy for diagnosing and treating sleep apnea is still relatively unexplored. Hence, there is a continuing need to improve the techniques for applying pacing therapy from implantable cardiac devices in a manner that effectively combats sleep apnea and heart failure.